Project Summary Although children in recent birth cohorts (born 2008 to 2010) have lower obesity rates than earlier cohorts, the high rates of obesity among children and adolescents in the U.S. remain a clinical and public health emergency. Understanding prenatal and early life determinants of upward growth trajectories and resultant obesity is a priority for preventing childhood obesity. The CCCEH published the first human data showing that childhood obesity risk through age 7 was associated with prenatal exposures to airborne polycyclic aromatic hydrocarbons (PAH); an effect that persists in our ongoing follow-up of the cohort to age 12 and is consistent with recent animal and other epidemiologic data. Here we propose to follow-up 350 of the cohort children to age 15-17 years for obesity outcomes using MRI scans to measure abdominal visceral adipose tissue (VAT) mass, the component of total fat mass most directly linked to future health risks. This work will determine whether the effects of prenatal PAH exposures on childhood adiposity continue into adolescence; overweight or obesity that persists from childhood into adolescence is likely to continue into adulthood. We will assess the extent to which PAH exposure related increases in weight reflect gains in VAT, the fat deposit that most directly places individuals at increased risk for cardiovascular disease, Type II diabetes, sleep apnea, acid reflux and obesity related cancers. We have also been measuring neurocognitive outcomes in the cohort children throughout childhood and we find that higher adiposity and poorer emotional self-regulation co-occur in the children. Integrating the three proposed projects we propose to investigate the role of prenatal PAH exposures in the development of a cluster of outcomes that encompass obesity and deficits in self-regulation of thought, emotion, and behavior. At age 15-17 we will also collect data on hedonic eating behaviors, including eating as a coping mechanism, emotional eating, binge eating, and food addiction; patterns of eating that we hypothesize will be associated with deficits in self-regulation. We will collect data on sedentary behaviors which are also hypothesized to be related to deficits in self-regulation. The proposed work will establish whether a cluster of outcomes occurs in adolescence that is characterized by greater adiposity, higher hedonic eating behavior, sedentary pursuits, and poorer neuropsychological function on measures of self-regulation and poorer behavioral and emotional function. Lastly using MRI brain scan data previously collected when the children were 9-12 years old, we will determine whether structural and functional differences can be identified in the children?s brains that mediate links between prenatal PAH exposures and these obesity related and neurodevelopmental outcomes in adolescence. Evidence that PAH exposures are part of the multi-factorial set of determinants of obesity risk will provide new avenues for obesity prevention that can be incorporated into multi-level, systems-based approaches to preventing obesity. The birth cohort analyses proposed here are unique and this is the only study population in which these mechanistic hypotheses can be tested.